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lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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Types of RNA01:20

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Three main types of RNA are involved in protein synthesis: messenger RNA (mRNA), transfer RNA (tRNA), and ribosomal RNA (rRNA). These RNAs perform diverse functions and can be broadly classified as protein-coding or non-coding RNA. Non-coding RNAs play important roles in regulating gene expression in response to developmental and environmental changes. Non-coding RNAs in prokaryotes can be manipulated to develop more effective antibacterial drugs for human or animal use.
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Proteins that regulate transcription can do so either via direct contact with RNA Polymerase or through indirect interactions facilitated by adaptors, mediators, histone-modifying proteins, and nucleosome remodelers. Direct interactions to activate transcription is seen in bacteria as well as in some eukaryotic genes. In these cases, upstream activation sequences are adjacent to the promoters, and the activator proteins interact directly with the transcriptional machinery. For example, in...
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Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
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Related Experiment Video

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Author Spotlight: An Integrated Workflow to Study the Promoter-Centric Spatio-Temporal Genome Architecture in Scarce Cell Populations
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Long non-coding RNAs direct the SWI/SNF complex to cell type-specific enhancers.

James A Oo1,2,3, Timothy Warwick1,2,3, Katalin Pálfi1

  • 1Goethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.

Nature Communications
|January 2, 2025
PubMed
Summary
This summary is machine-generated.

Long non-coding RNAs (lncRNAs) guide the SWItch/Sucrose Non-Fermentable (SWI/SNF) complex to specific enhancers. This lncRNA-SWI/SNF interaction controls chromatin accessibility and gene expression, revealing a new regulatory mechanism.

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Chromatin Isolation by RNA Purification ChIRP
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Area of Science:

  • Molecular Biology
  • Genomics
  • Epigenetics

Background:

  • Chromatin remodeling is crucial for DNA accessibility and gene expression.
  • The SWItch/Sucrose Non-Fermentable (SWI/SNF) complex is vital for context-dependent gene regulation.
  • Mechanisms guiding SWI/SNF to specific genomic locations remain unclear.

Purpose of the Study:

  • To elucidate the mechanisms directing SWI/SNF to specific genomic targets.
  • To investigate the role of long non-coding RNAs (lncRNAs) in SWI/SNF targeting.
  • To understand how lncRNA-SWI/SNF interactions influence chromatin accessibility and gene expression.

Main Methods:

  • Demonstration of trans-acting lncRNAs directing SWI/SNF to enhancers.
  • Analysis of SWI/SNF binding preferences for lncRNAs.
  • Assessment of lncRNA and SWI/SNF co-localization at enhancers.
  • Knockdown experiments to observe effects on SWI/SNF distribution and gene expression.

Main Results:

  • SWI/SNF preferentially binds lncRNAs, which then bind DNA targets in trans.
  • lncRNAs and SWI/SNF co-localize at cell type-specific enhancers.
  • Knockdown of lncRNAs causes SWI/SNF redistribution and differential gene expression.
  • lncRNA-SWI/SNF-enhancer networks support an enhancer hub model.

Conclusions:

  • lncRNAs competitively recruit SWI/SNF to specific enhancers.
  • This provides a dynamic regulatory layer for chromatin accessibility.
  • lncRNAs are key mediators of enhancer activity and gene expression through SWI/SNF recruitment.